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The effects of exercise training on Kinesin and GAP-43 expression in skeletal muscle fibers of STZ-induced diabetic rats.

ABSTRACT: Kinesin-1 and Growth Associated Protein 43 (GAP-43) localization in muscle fiber are crucial for proper skeletal muscle hypertrophy. To evaluate this assumption, we investigated the beneficial effects of endurance training on GAP-43 and Kinesin Family Member 5B (KIF5B) expression in gastrocnemius muscle of streptozotocin (STZ)-induced diabetic rats. Fifty-two male rats were randomly divided into four groups: healthy control (C), healthy trained (T), diabetic control (DC) and diabetic trained (DT). Diabetes was induced by a single intraperitoneal injection of STZ (45 mg/kg). The rats in DT and T groups were subjected to treadmill running for 5 days a week over 6 weeks. The results indicated that the GAP-43 and KIF5B protein levels in the DC group were significantly lower than those in the C group. Additionally, chronic treadmill running in diabetic rats was accompanied by significant increase of GAP-43 and KIF5B protein expression, compared to DC group. Furthermore, the endurance training in healthy rats was associated with a significant increase of GAP-43 and KIF5B protein levels. In addition, we found positive correlation between GAP-43 and KIF5B protein levels and myonuclear number per fiber and average gastrocnemius cross-sectional area (CSA). GAP43 and KIF5B protein levels were decreased in skeletal muscles of diabetic rats, and exercise training had beneficial effects and could restore their abnormal expression. Moreover, there is a strong relationship between muscle hypertrophy and GAP-43 and KIF5B protein levels.

SUBMITTER: Rahmati M

PROVIDER: S-EPMC8099856 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundSodium-glucose cotransporter 2 inhibitors (SGLT2i) are commonly used in the management of type 2 diabetes mellitus (T2DM) and have been found to worsen the reduction of skeletal muscle mass in individuals with T2DM. This study aims to examine the potential of exercise in mitigating the skeletal muscle atrophy induced by SGLT2i treatment.MethodsA rat model of T2DM (40 male Sprague-Dawley rats; T2DM induced by a combination of high-fat diet and streptozotocin) was used to examine the effects of six-week treatment with Dapagliflozin (DAPA, SGLT2i) in combination with either aerobic exercise (AE) or resistance training (RT) on skeletal muscle. T2DM-eligible rats were randomized into the T2DM control group (CON, n = 6), DAPA treatment group (DAPA, n = 6), DAPA combined with aerobic exercise intervention group (DAPA + AE, n = 6), and DAPA combined with resistance training intervention group (DAPA + RT, n = 6). To assess the morphological changes in skeletal muscle, myosin ATPase and HE staining were performed. mRNA expression levels of Atrogin-1, MuRF1, and Myostatin were determined using quantitative PCR. Furthermore, protein expression levels of AKT, p70S6K, mTOR, FoXO1/3A, NF-κB, and MuRF1 were examined through western blotting.ResultsBoth the administration of DAPA alone and the combined exercise intervention with DAPA resulted in significant reductions in blood glucose levels and body weight in rats. However, DAPA alone administration led to a decrease in skeletal muscle mass, whereas RT significantly increased skeletal muscle mass and muscle fiber cross-sectional area. The DAPA + RT group exhibited notable increases in both total protein levels and phosphorylation levels of AKT and p70S6K in skeletal muscle. Moreover, the DAPA, DAPA + AE, and DAPA + RT groups demonstrated downregulation of protein expression (FoXO1/3A) and mRNA levels (Atrogin-1, MuRF1, and Myostatin) associated with muscle atrophy.ConclusionsOur findings provide support for the notion that dapagliflozin may induce skeletal muscle atrophy through mechanisms unrelated to protein metabolism impairment in skeletal muscle, as it does not hinder protein metabolic pathways while reduces muscle atrophy-related genes. Additionally, our observations reveal that RT proves more effective than AE in enhancing skeletal muscle mass and muscle fiber cross-sectional area in rats with T2DM by stimulating protein anabolism within the skeletal muscle.

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The effects of exercise training on Kinesin and GAP-43 expression in skeletal muscle fibers of STZ-induced diabetic rats.

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